involved in determining susceptibility to crohns disease参与确定克罗恩病的易感因素课件

Crohns Disease By: Jaspreet Deol, Laila Rkieh, Marice Zakhari, Sahar Noorzad PHM142 Fall 2012 Coordinator: Dr. Jeffrey Henderson Instructor: Dr. David Hampson Inflammatory Bowel Disease (IBD) Inflammation, swelling, and irritation of GI tract Approximately 0.5% of the Canadian population have an IBD, highest reported prevalence rate Jewish, highest risk; African Americans, lower risk Prognosis: condition marked by periods of improvement followed by flare-ups Diagnosed between ages 13-30 Autoimmune disease Decreased suppression of immune response for enteric bacteria and self-antigens CROHNS DISEASE SYMPTOMATOLOGY Pain/cramps Caused by strictures (narrowing of the GI tract) Narrowed passageway due to chronic inflammation and the formation of scar tissue Bowel obstruction nausea, vomiting Diarrhea Rectal bleeding Anemia (Pernicious/Dietary) Weight loss, reduced appetite Fever, fatigue, skin lesions, join pain, delayed growth in children COMPLICATIONS Bowel obstruction Complete/partial intestinal blockage caused by inflammation and accumulation of scar tissue Ulcers Chronic inflammation leading to holes/breaks in GI wall Fistulas Tunnels penetrating through the intestinal wall into surrounding tissue External vs. Internal Anal fissure Malnutrition Colon cancer Arthritis, inflammation of eyes/skin, kidney stones, gall stones, inflammation of bile ducts TYPES Ileocolitis* Ileitis Gastroduodenal Crohns disease Jejunoileitis Crohns granulmatous colitis DIAGNOSTIC TESTS PHYSICAL EXAMINATION INDICATORS: 1.Blood test WBC count: elevated with inflammation management involves treatment of active disease and maintenance of remission Antibiotics, anti-inflammatory and immunosuppressant drugs can be included in treatment Monoclonal antibodies are administered for neutralization of TNF-a to combat inflammation and fistulising disease; Infliximab (Remicade)mouse-human chimeric, Adalimumab (HUMIRA)human References Balfour, S.R. (2007). Bacteria in Crohns disease: mechanisms of inflammation and therapeutic implications. Journal of Clinical Gastroenterology, 41, S37-S43. Bernsetin C., Blanchard, J., Fedorak, R., Israel, D., Jackson, M., Koehoorn, M., MacKenzie, A., Svenson, L., & Wajda, A. (2006). The epidemiology of inflammatory bowel disease in Canada: a population-based study. American Journal of Gastroenterology, 101 (7), 1559-1568. Crohns Disease. (2012). In A.D.A.M. Medical Encyclopedia online. Retrieved from /pubmedhealth/PMH0001295/ Crohns and Colitis Foundation of America. (2012). Types of Crohns Disease and Associated Symptoms. Retrieved from /what-are-crohns-and-colitis/what-is-crohns-disease/types-of-crohns-disease.html Goa, B., Saba, T.M., Tsan, M.F. (2002). Role of v3-integrin in TNF-induced endothelial cell migration. American Journal of Physiology, 283,C1196-C1205. Henderson, J. Hypomethylation, Folic Acid Metabolism, and Vitamin B12 PDF Document. Retrieved from Lecture Notes Online Website: http:/phm.utoronto.ca/jeffh/phmunit4cb.pdf Kanai, M., Mullen, C., Podolsky, D.K. (1997). Intestinal trefoil factor induces inactivation of extracellular signal-regulated protein kinase in intestinal epithelial cells. American Journal of Physiology, 95, 178-182. Mayo Foundation for Medical Education and Research. (2011). Crohns Disease. Retrieved from /health/crohns-disease/ Mzes, G., Molnr, B., Tulassay, Z., and Sipos, F. (2012). Changes of the cytokine profile in inflammatory bowel diseases. World Journal of Gastroenterology, 18(41), 5848-5861. National Digestive Diseases Information Clearinghouse. (2011). Crohns Disease (NIH Publication No. 12-3410). Betheseda, MD: U.S. Sengupta, N., MacDonald, T.T. (2007). The role of matrix metalloproteinases in stromal/epithelial interactions in the gut. Physiology, 22(6), 401-409. Shanahan, F. (2002). Crohns Disease. The Lancet, 359, 62-69. Retrieved from: http:/journals1.scholarsportal.in